Neurobehavioral Effects of Prevalent Neurotoxicants in Children: A Cohort Study of the Cincinnati Center for Children's Environmental Health

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Cincinnati,
Ohio45229

Purpose:

The goal of the HOME Study is to quantify the impact of low-level fetal and early childhood
exposures to environmental toxicants including lead, mercury, and other metals, pesticides,
polychlorinated biphenyls (PCBs), persistent organic pollutants (PBDEs/PFCs), phthalates,
phenols, environmental tobacco smoke, and alcohol on child development, neurobehavior,
health, and growth. The HOME Study will also evaluate meconium as a biomarker for fetal
exposure and test the effectiveness of home repairs to control lead hazards and injuries in
early childhood.

Study summary:

This study aims to examine the effects of low-level exposures to prevalent neurotoxicants on
health, growth, and neurobehavior among a representative sample of children. Pregnant women
were enrolled in the project around 16 weeks of gestation. In the first phase of the study,
we followed children resulting from the pregnancy through the age of 36 months. The second
phase extended follow-up through 72 months. Phase 3 extended follow-up to 8 years (range
7.5-10) with comprehensive neurobehavioral assessments. Phase 4 will allow follow-up at 12
years (range 11-13), and includes measures of health, growth and body composition, behavior
and mental health, and neuroimaging. To address the potential adverse health risks of
environmental chemicals, including persistent pollutants such as PBDEs and PFCs and other
non-persistent chemicals, on fetal, infant, and child neurobehavior, the investigators are
systematically examining their associations with endocrine function, cognition, learning and
memory, motor skills, attention and executive function, and behavior from age 1 to 7.5-10
years. The investigators are also examining exposures at different developmental stages (in
utero at 16 weeks of gestation, early childhood, school age, preadolescence) using stored
biological samples and measure child neurobehavior at 1, 2, 3, 4, 5, 8, and 12 years. This
longitudinal study will allow the investigators to determine the dose response, windows of
susceptibility, and persistence of the association. The investigators are also examining the
contribution of PBDE exposures from house dust in a subset of children who have complete
sets of samples of maternal serum and child serum collected from annual visits along with
extensive measures of mouthing behaviors.
Hypotheses from the four phases of the study are as follows:
1. In utero exposures measured by survey (alcohol and ETS), maternal and cord blood (lead
and mercury) maternal and cord serum (ETS), and urine (pesticides) are less predictive
of in utero effects of prevalent toxicants, including cognition, behavior problems, and
growth compared with the same toxicants in meconium.
2. Prenatal and postnatal exposures to prevalent pesticides and ETS are associated with
adverse neurobehavioral effects, and growth delay in children.
3. Higher lead exposure, measured during pregnancy and early childhood using maternal
blood, cord blood, meconium and children's blood, will be associated with lower IQ
scores and more behavioral problems for children with a maximal blood lead level < 5
mg/dL.
4. Children in the lead treatment arm will have: blood lead that is 2.7 mg/dL lower,
higher IQ scores, greater growth velocity, and fewer behavioral problems than children
in the control group.
5. Levels of lead in dust, soil and water will be significantly lower for housing units in
the lead treatment arm compared with the injury control arm at 36 and 48 month home
visits.
6. A multifactorial, housing intervention will reduce residential injury by 30 percent
among children in the injury treatment arm compared with those in the lead treatment
arm.
7. Prenatal and Postnatal exposures to PBDEs and PFCs are associated with altered thyroid
hormone levels and deficits in infant and child neurobehavior
8. With increasing child age, PBDE exposure from household dust becomes a stronger
predictor of child serum PBDE concentration than exposure from placenta or breast milk.
9. Developmental PBDE and PFC exposures are associated with internalizing symptoms.
10. Developmental PBDE and PFC exposures are associated with adverse changes in anatomical
structure, neurochemistry, organization of white matter tracts, and connectivity of
neural networks.
11. PFAS affect the gene expression and function of several biological pathways that
program the fetus/infant towards a 'thrifty phenotype'. This leads to accelerated early
childhood growth, increased fat mass, and features of metabolic syndrome.